Sunday, March 26, 2017

The pathology of evolution

Aaron posted the link to this paper via Facebook:

Selection in Europeans on Fatty Acid Desaturases Associated with Dietary Changes

As the authors comment in the discussion:

"Agricultural diets would have led to a higher consumption of grains and other plant-derived foods, relative to huntergatherer populations. Alleles that increase the rate of conversion of SC-PUFAs to LC-PUFAs would therefore have been favored".

Or to rephrase it slightly, from the legend of Fig 6:

"The adoption of an agricultural diet would have increased LA and decreased ARA and EPA consumption, potentially causing a deficiency in LC-PUFAs".

This is something I have thought about, in more general terms, for some time.

At the time of the switch from hunting animals for their fat to growing grains for their starch the paper suggests that there was a population-wide potential deficiency of the longer chain PUFA, arachidonic acid, EPA and DHA.

This applied a selection pressure to the population. Within the population there was a random distribution of the ability to elongate and desaturate linoleic and alpha linolenic acids to their longer chain derivatives.

People who had this ability in generous amounts did well. Those without, didn't.

What happened to those people who were "without" the lucky gene snps to survive well without animal derived lipids? They didn't "develop" the genes, no individual suddenly develops a better gene. Their intrinsic inability means they didn't reproduce as successfully.

Their genes are currently under represented in the gene pool today.

It has always struck me that the process of getting poorly adapted genes out of the gene pool is what we describe as pathology, illness. Trying to patch it up is what we call medicine. Individuals don't adapt. They either do well or badly. The population "adapts" through the illnesses of those whose genes are not appropriate to the new environment.

The adaptation of our species to the novel situation of agriculture is far from complete. On-going adaptation of a species to a new environment is via the suffering of the individuals with genes more appropriate to the previous long term stable environment. The default for a person with on-going pathology might be to step back 10,000 years rather than continuing to assist evolution of the species via personal pathology. A lot of pathology will be needed.

Miki Ben-Dor has a nice post along these lines this on his blog.


Of course the adaptation to sucrose and bulk seed oils has only just begun. LOTS of pathology needed to adapt the species to those two! Juvenile onset type 2 diabetes is what we call the process.


LA_Bob said...

Ishmael could not be reached for comment.

karl said...

There are background bits in that paper that don't pass --

"With large brains composed mostly of lipids, humans have a particularly strong requirement for these fatty acids "


"These SC-PUFAs are considered essential and are obtained primarily through the consumption of vegetable oils."

The actual 'requirement' remains unknown. The paper that was showing LA as essential has grave problems - confounded with a lack of O-3.

"...and to risks of cardiovascular and coronary heart disease and mortality "

We now know that the Keys study data the was hidden shows the opposite.

Anyway - even if there is a dietary 'requirement' - it is tiny compared to what the average American eats.


That being said - it is obvious that evolution has not caught up with the huge change that started in 1960 with ever increasing consumption of concentrated seed oils.

karl said...

You post also brings some much needed background to the idea of "what is a healthy diet?"

Really depends on your genes. It is pretty obvious that some people don't tolerate lactose - the effect is rather quick - but other carbohydrates the problems may happen much slower.

My father, even when he was in his late 80's had excellent postprandial BG after eating a fairly high carb meal. If I don't have that ability - is it due to mDNA selection of just my mix of genes?

Then there is the new high PUFA diets - no one has yet to adapt - but I would be surprised if there wasn't a spread of tolerance.

So if what makes a perfect diet depends on one's genes, it means it is over due to discount those pushing ungrounded narratives or parroting the most fashionable diet.


I go to this gymnasium center where lots of 18-22yr/olds are playing basketball/volleyball etc. I keep wondering why their skin looks older than their years and even these active kids have muscles that look floppy and flaccid compared with my aging memory of my peers from when I was that age. Is it my imagination or is this generation particularly unhealthy? Is it from eating vast amounts of seed-oil? Or some endocrine disruptor? ( I've been scanning old film from the 50's and 60's - really seems to me that there is a difference - but I'm not sure).

raphi said...

Hi Peter,

The concept of evolutionary mismatch is so elegant and powerful it's a damn shame medical professionals and biologists pay so little attention to it. How pathology, at the population level, is discussed in a manner completely oblivious to selection pressures boggles my mind...

If anyone is interested in Chris Mastejohn's 2008 analysis of the essentiality of fatty acids, see here

According to him, "the requirement [of AA & DHA] for growing animals appears to be less than one percent in all species and less than 0.5 percent in most circumstances".

I thought some of you might find his explanation poor body temperature regulation upon EFA deficiency interesting:

"In EFA deficiency, the ETC fails to efficiently pump the hydrogen ions in the first place and fails to make the ATP (32, 33). This is like poking holes in the bucket – the water still spills, but the cups never get full. The live organism engages in a number of adaptations to try to conserve its capacity to make ATP, but the net availability of this critical energy molecule is still depleted (34). The body temperature of the EFA-deficient animals never rises (23), probably because the heat leaves as the water evaporates through the skin. The metabolic rate decreases to normal or even below normal after four months, and is actually increased at all time points with curative doses of EFAs (23); this is the opposite of what we would expect but probably occurs because the measurement is adjusted for surface area rather than lean body mass, and part of the loss of bodyweight in EFA deficiency may represent the wasting of metabolically active muscle tissue and part of the gain during EFA repletion may represent the rebuilding of this tissue. Thus thyroid hormone seems to aggravate EFA deficiency by increasing the need for arachidonate, but a hypersensitivity to it does not seem to be involved in the basic presentation of the deficiency. Rather, defective ETC functioning effectively leads to starvation in spite of the increased food intake because of an inability to harness the energy provided by it."

Peter said...

raphi, interesting. PUFA uncouple but fail to generate maintain body temperature (explained by heat lost through water evaporation via non waterproofed skin). But metabolic rate, presumably calculated from O2 consumption, ends up depressed. In uncoupled animals which are cold??????? Go figure! Chris has never struck me as a thinking person so I'd be wide open for other explanations.

Oh boy, oops. Ref 34. Notice there is no title along side the ref, unlike the rest of the refs. Here is the title

Mitochondrial Adaptation to in vivo Polyunsaturated Fatty Acid Deficiency: Increase in Phosphorylation Efficiency.

and from the abstract at

"Despite identical respiratory rate and in situ mitochondrial membrane potential (ΔΨ), mitochondrial and cytosolic ATP/ADP–Pi ratios were significantly higher in PUFA-deficient cells than in control cells treated with DNP. We show that PUFA-deficient cells display an increase of phosphorylation efficiency, a higher mitochondrial ATP/ADP–Pi ratio being maintained despite the lower ΔΨ".

I think I might be cautious about Chris' ideas. And always check his citations (especially any he skips the title of)...


Passthecream said...

After reading Miki's post I watched one of the Ungar presentations which led to a simple thought (the only kind available to me). I suppose that it's possible to track the time of occurrence of the increase in copies of the amylase gene however if the Homo lineage arose as a specialised version of the earlier Australopithecines, losing generality by moving to carnivory, there may have been a period where the number of amylase gene repeats was decreasing --- evolution and devolution being the same process, responding appropriately to changing conditions.

Peter said...

Pass, yes, there may well have been problems adapting to a fat based diet. But the non fat adapted people will have been weeded out well before 10,000 years ago. The very rapid change is to grains where adaptation is needed currently, and slightly more slowly to starches which will have been around for a little longer...


Passthecream said...

Yes, the pre-homo lineages were far too long ago for that generality to prevail. But perhaps the pressures which led to our specialisation were another one of the many bottlenecks that our species seems to have experienced.

There's an idea that when a population gets above a certain size then genes don't easily disappear, they just keep shuffling about. (I know how they must feel). In the absence of strong evolutionary pressures there is just a general drift. The pathology of inappropriate genes vs environment would be chronic. Among the various slow acting selection pressures there must also be one along the lines of : the individuals most capable of finding the best possible foodstuffs vs their genetics are more fit, will prosper.

Hopefully that's us.

Another of Miki's posts focuses on the time spent by hunter-gatherers per kilojoule harvested with eg large mammals being 10 times more efficient than uso's. Interesting to see reptiles being quite high on the list too. It is much more complex, and controversial, to work out how many kj/hour of effort different foods provide now but I have a suspicion that those higher up our lists will be the ones which use more fossil fuel energy in their production. Its a bit like eating coal.

Puddleg said...

Supposing you've adapted to low intakes of EPA, DHA, AA on a cereal-based peasant diet (because the rest of your family has died of the plague, but no matter). You can make these VLCPUFAs efficiently from the traces of LA and ALA in the grains and legumes.
A few hundred years on your descendants are eating chips fried in corn oil. With those genes you passed on, they can now make more AA on a daily basis than any amount ever consumed on a daily basis before.
One generation's adaptation is another generation's maladaptation.

Peter said...

True George...

Passthecream said...

George, over the space of a few hundred years many different lines of inheritance are shuffled. In large populations this conserves the diversity. Even though your gt gt gt gt gt gt grandfathers siblings may have died before passing on their DNA, as many as 256 other contemporary individuals constitute your heritage. Only fewer than that if some of them were the same person, and the situation you describe would apply to a long term isolated group of not many individuals.

I still agree emphatically about the inappropriateness of most 'civilized' foodstuffs. The economics of food production has gone far away from producing nutrients that our systems can cope with.

Puddleg said...

Yes I've made the example personal, and about survival rather than fertility and competitiveness, because it's funnier that way, but the evidence for it happening on a large scale, based on variations between regional populations with different historical dietary habits is good; and of course the mode of evolution is just the fate of individuals in the mass; these adaptations can be driven through the majority of a large area's population in this way.

Aren't, like, hundreds of my ancestors Genghis Khan anyway?

Passthecream said...

I was thinking Atila H. in my case but looks like Edward III might figure in there somewhere.


Passthecream said...

I can't remember where I learned it, a probability and statistics course I suspect, but the example was that it only takes as few as 50 breeding individuals in a population to conserve genetic diversity. Snm's aside and that was before mito-dna was thought about much. It is easy to imagine a bottleneck population of, say, less than 50 experiencing a great deal of evolutionary pressure , and adapting to it, might then re-emerge and shuffle their new genetic contribution back into a larger population, conserving it. Whilst the mechanism is radically different, there is still an echo of the way that bacteria exchange genetic material.

Puddleg said...

We've traced my girlfriend's rare family name right back to a pale descendant of Charles II.
This actually makes her a descendant of Mary Queen of Scots and thus my rightful monarch.
Her friend, meanwhile, traced her own ancestry back to Oliver Cromwell.